Research: Virus infection worsens the condition in Vormies

Researchers say that an infection with a common virus that can be transferred to Fötus before the birth of mother is considerably deteriorating a fatal complication of early birth in experiments with mice.

The research team and by the National Institutes of Health, which is understood by John's Hopkins Children's Center, is financed by the new findings that search for better treatments for NEC – a relatively rare illness, but still the most common intestinal complication in orns.

A report on the study published on February 13 in cellular and molecular gastroenterology and hepatology.

“NEC is the most important disease that most people have probably never heard of. The effects of this disease on premature babies and their families are great and are deteriorated by the fact that people often hear the lover for the first time after their first time Surprisingly, people will not know what causes NEC primarily. Professor of pediatric surgery at the Johns Hopkins University School of Medicine and surgeon and co-director of the Johns Hopkins Children's Center.

Up to 10% of the early infants develop a NEC, an illness that is characterized by severe inflammation of the intestinal mucosa that this tissue ultimately kills. About a third of the babies with NEC ultimately dies, and the survival rates have remained unchanged in the past three decades.

Latest studies in animals, according to Hackam, has shown that the brand ignition of NEC is at least partially due to a continued increase in an immune protein called Toll-Like receptor 4 (TLR4), which is activated by the abnormal accumulation of specific intestinal bacteria that tenden tend to overgrow the digestion of early infants. But why NEC is more serious for some babies and tends to strike was a mystery.

This has led to CMV as a suspect, says Hackam.

An estimated 40% to 80% of people worldwide are chronically infected with cytomegalovirus, a virus in the herpes family, which usually does not cause symptoms in healthy people, but is a common cause of hearing loss and other birth errors in organ damage if they are transferred from Fetus during pregnancy. Feten acquire CMV of infected mothers during pregnancy in 30% to 50% of cases.

Hackam and his colleagues suspect a connection between CMV and NEC heavy and developed a NEC model for newborns with CMV. When they compared the intestine of rodents with and without CMV infection, they found that mice that houses CMV, had a significantly poorer tissue damage and higher mortality rates compared to those without this virus.

In search of a molecular mechanism for this result, the researchers compared the genetic activity in the intestine of the two groups of mice. They found that a CMV infection triggered genetic paths, which encouraged inflammation, disrupted the metabolism and caused the cells to make more TLR4.

A closer look showed that CMV also damaged mitochondria, organelles that serve as energy abrasions for the cells. The damage reduced the mitochondrial production of adenosine triphosphate (ATP) significant, a molecule that use cells for fuel.

Other experiments with mouse tissue showed that TLR4 was necessary for each of these effects. Mice that have been genetically changed, for example not to produce a TLR4 in their intestine, had a significantly lower NEC thread level even in CMV infections, which indicates that this protein could be a good goal for the development of medication against NEC.

If animal and human studies confirm the CMV-NEC connection, another treatment option could be to give adenosine, explains Hackam, a forerunner for ATP that is usually sold as a nutritional supplement. When the researchers gave mice with NEC and CMV -adenosin, this significantly reduced the NEC -heavy. The team plans to examine these ideas in future studies.

Other Johns Hopkins researchers who contributed to this study Seong Jang, Sierra Williams-McLeod, Asuka Ishiyama, Steve N. Steinway, Sanxia Wang, Menghan Wang, Thomas Prindle Jr. and William B. Fulton.

This study was financed by grants from the National Institutes of Health (R35 GM141956 and T32 DK007713) and the Garrett Fund for the surgical treatment of children at John's Hopkins University.

Hackam and Sodhi consider patents to develop new active ingredients to inhibit TLR4 for the prevention and treatment of NEC.